Activation of nuclear factor-kappa B signalling promotes cellular senescence View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2011-05

AUTHORS

Emilie Rovillain, Louise Mansfield, Catia Caetano, Monica Alvarez-Fernandez, Otavia L. Caballero, Rene H. Medema, Holger Hummerich, Parmjit S. Jat

ABSTRACT

Cellular senescence is a programme of irreversible cell cycle arrest that normal cells undergo in response to progressive shortening of telomeres, changes in telomeric structure, oncogene activation or oxidative stress. The underlying signalling pathways, of major clinicopathological relevance, are unknown. We combined genome-wide expression profiling with genetic complementation to identify genes that are differentially expressed when conditionally immortalised human fibroblasts undergo senescence upon activation of the p16-pRB and p53-p21 tumour suppressor pathways. This identified 816 up and 961 downregulated genes whose expression was reversed when senescence was bypassed. Overlay of this data set with the meta-signatures of genes upregulated in cancer showed that nearly 50% of them were downregulated upon senescence showing that even though overcoming senescence may only be one of the events required for malignant transformation, nearly half of the genes upregulated in cancer are related to it. Moreover 65 of the up and 26 of the downregulated genes are known downstream targets of nuclear factor (NF)-κB suggesting that senescence was associated with activation of the NF-κB pathway. Direct perturbation of this pathway bypasses growth arrest indicating that activation of NF-κB signalling has a causal role in promoting senescence. More... »

PAGES

2356

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/onc.2010.611

DOI

http://dx.doi.org/10.1038/onc.2010.611

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1041112885

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/21242976


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